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Advanced glycation endproducts, dityrosine and arginine transporter dysfunction in autism - a source of biomarkers for clinical diagnosis / A. ANWAR in Molecular Autism, 9 (2018)
[article]
Titre : Advanced glycation endproducts, dityrosine and arginine transporter dysfunction in autism - a source of biomarkers for clinical diagnosis Type de document : Texte imprimé et/ou numérique Auteurs : A. ANWAR, Auteur ; P. M. ABRUZZO, Auteur ; S. PASHA, Auteur ; K. RAJPOOT, Auteur ; A. BOLOTTA, Auteur ; A. GHEZZO, Auteur ; M. MARINI, Auteur ; A. POSAR, Auteur ; Paola VISCONTI, Auteur ; P. J. THORNALLEY, Auteur ; N. RABBANI, Auteur Article en page(s) : 3p. Langues : Anglais (eng) Mots-clés : Advanced glycation endproducts (AGEs) Amino acid metabolome Autism spectrum disorder (ASD) Machine learning Oxidative stress Ferrara (CE BIF) Index. décimale : PER Périodiques Résumé : Background: Clinical chemistry tests for autism spectrum disorder (ASD) are currently unavailable. The aim of this study was to explore the diagnostic utility of proteotoxic biomarkers in plasma and urine, plasma protein glycation, oxidation, and nitration adducts, and related glycated, oxidized, and nitrated amino acids (free adducts), for the clinical diagnosis of ASD. Methods: Thirty-eight children with ASD (29 male, 9 female; age 7.6 +/- 2.0 years) and 31 age-matched healthy controls (23 males, 8 females; 8.6 +/- 2.0 years) were recruited for this study. Plasma protein glycation, oxidation, and nitration adducts and amino acid metabolome in plasma and urine were determined by stable isotopic dilution analysis liquid chromatography-tandem mass spectrometry. Machine learning methods were then employed to explore and optimize combinations of analyte data for ASD diagnosis. Results: We found that children with ASD had increased advanced glycation endproducts (AGEs), Nepsilon-carboxymethyl-lysine (CML) and Nomega-carboxymethylarginine (CMA), and increased oxidation damage marker, dityrosine (DT), in plasma protein, with respect to healthy controls. We also found that children with ASD had increased CMA free adduct in plasma ultrafiltrate and increased urinary excretion of oxidation free adducts, alpha-aminoadipic semialdehyde and glutamic semialdehyde. From study of renal handling of amino acids, we found that children with ASD had decreased renal clearance of arginine and CMA with respect to healthy controls. Algorithms to discriminate between ASD and healthy controls gave strong diagnostic performance with features: plasma protein AGEs-CML, CMA-and 3-deoxyglucosone-derived hydroimidazolone, and oxidative damage marker, DT. The sensitivity, specificity, and receiver operating characteristic area-under-the-curve were 92%, 84%, and 0.94, respectively. Conclusions: Changes in plasma AGEs were likely indicative of dysfunctional metabolism of dicarbonyl metabolite precursors of AGEs, glyoxal and 3-deoxyglucosone. DT is formed enzymatically by dual oxidase (DUOX); selective increase of DT as an oxidative damage marker implicates increased DUOX activity in ASD possibly linked to impaired gut mucosal immunity. Decreased renal clearance of arginine and CMA in ASD is indicative of increased arginine transporter activity which may be a surrogate marker of disturbance of neuronal availability of amino acids. Data driven combination of these biomarkers perturbed by proteotoxic stress, plasma protein AGEs and DT, gave diagnostic algorithms of high sensitivity and specificity for ASD. En ligne : http://dx.doi.org/10.1186/s13229-017-0183-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=354
in Molecular Autism > 9 (2018) . - 3p.[article] Advanced glycation endproducts, dityrosine and arginine transporter dysfunction in autism - a source of biomarkers for clinical diagnosis [Texte imprimé et/ou numérique] / A. ANWAR, Auteur ; P. M. ABRUZZO, Auteur ; S. PASHA, Auteur ; K. RAJPOOT, Auteur ; A. BOLOTTA, Auteur ; A. GHEZZO, Auteur ; M. MARINI, Auteur ; A. POSAR, Auteur ; Paola VISCONTI, Auteur ; P. J. THORNALLEY, Auteur ; N. RABBANI, Auteur . - 3p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 3p.
Mots-clés : Advanced glycation endproducts (AGEs) Amino acid metabolome Autism spectrum disorder (ASD) Machine learning Oxidative stress Ferrara (CE BIF) Index. décimale : PER Périodiques Résumé : Background: Clinical chemistry tests for autism spectrum disorder (ASD) are currently unavailable. The aim of this study was to explore the diagnostic utility of proteotoxic biomarkers in plasma and urine, plasma protein glycation, oxidation, and nitration adducts, and related glycated, oxidized, and nitrated amino acids (free adducts), for the clinical diagnosis of ASD. Methods: Thirty-eight children with ASD (29 male, 9 female; age 7.6 +/- 2.0 years) and 31 age-matched healthy controls (23 males, 8 females; 8.6 +/- 2.0 years) were recruited for this study. Plasma protein glycation, oxidation, and nitration adducts and amino acid metabolome in plasma and urine were determined by stable isotopic dilution analysis liquid chromatography-tandem mass spectrometry. Machine learning methods were then employed to explore and optimize combinations of analyte data for ASD diagnosis. Results: We found that children with ASD had increased advanced glycation endproducts (AGEs), Nepsilon-carboxymethyl-lysine (CML) and Nomega-carboxymethylarginine (CMA), and increased oxidation damage marker, dityrosine (DT), in plasma protein, with respect to healthy controls. We also found that children with ASD had increased CMA free adduct in plasma ultrafiltrate and increased urinary excretion of oxidation free adducts, alpha-aminoadipic semialdehyde and glutamic semialdehyde. From study of renal handling of amino acids, we found that children with ASD had decreased renal clearance of arginine and CMA with respect to healthy controls. Algorithms to discriminate between ASD and healthy controls gave strong diagnostic performance with features: plasma protein AGEs-CML, CMA-and 3-deoxyglucosone-derived hydroimidazolone, and oxidative damage marker, DT. The sensitivity, specificity, and receiver operating characteristic area-under-the-curve were 92%, 84%, and 0.94, respectively. Conclusions: Changes in plasma AGEs were likely indicative of dysfunctional metabolism of dicarbonyl metabolite precursors of AGEs, glyoxal and 3-deoxyglucosone. DT is formed enzymatically by dual oxidase (DUOX); selective increase of DT as an oxidative damage marker implicates increased DUOX activity in ASD possibly linked to impaired gut mucosal immunity. Decreased renal clearance of arginine and CMA in ASD is indicative of increased arginine transporter activity which may be a surrogate marker of disturbance of neuronal availability of amino acids. Data driven combination of these biomarkers perturbed by proteotoxic stress, plasma protein AGEs and DT, gave diagnostic algorithms of high sensitivity and specificity for ASD. En ligne : http://dx.doi.org/10.1186/s13229-017-0183-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=354 Glyoxalase I polymorphism rs2736654 causing the Ala111Glu substitution modulates enzyme activity—implications for autism / Madhabi BARUA in Autism Research, 4-4 (August 2011)
[article]
Titre : Glyoxalase I polymorphism rs2736654 causing the Ala111Glu substitution modulates enzyme activity—implications for autism Type de document : Texte imprimé et/ou numérique Auteurs : Madhabi BARUA, Auteur ; Edmund C. JENKINS, Auteur ; Wenqiang CHEN, Auteur ; Salomon KUIZON, Auteur ; Raju K. PULLARKAT, Auteur ; Mohammed A. JUNAID, Auteur Année de publication : 2011 Article en page(s) : p.262-270 Langues : Anglais (eng) Mots-clés : autism glyoxalase I SNP advanced glycation endproducts (AGEs) receptor for advanced glycation end products (RAGEs) methylglyoxal Index. décimale : PER Périodiques Résumé : Autism is a pervasive, heterogeneous, neurodevelopmental disability characterized by impairments in verbal communications, reciprocal social interactions, and restricted repetitive stereotyped behaviors. Evidence suggests the involvement of multiple genetic factors in the etiology of autism, and extensive genome-wide association studies have revealed several candidate genes that bear single nucleotide polymorphisms (SNPs) in non-coding and coding regions. We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme. To identify the significance of the SNP, we have conducted functional assays for Glo1. We now present evidence that the presence of the A-allele at rs2736654 results in reduced enzyme activity. Glo1 activity is decreased in lymphoblastoid cells that are homozygous for the A allele. The Glu-isoform of Glo1 in these cells is hyperphosphorylated. Direct HPLC measurements of the glyoxalase I substrate, methylglyoxal (MG), show an increase in MG in these cells. Western blot analysis revealed elevated levels of the receptor for advanced glycation end products (RAGEs). We also show that MG is toxic to the developing neuronal cells. We suggest that accumulation of MG results in the formation of AGEs, which induce expression of the RAGE that during crucial neuronal development may be a factor in the pathology of autism. En ligne : http://dx.doi.org/10.1002/aur.197 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=141
in Autism Research > 4-4 (August 2011) . - p.262-270[article] Glyoxalase I polymorphism rs2736654 causing the Ala111Glu substitution modulates enzyme activity—implications for autism [Texte imprimé et/ou numérique] / Madhabi BARUA, Auteur ; Edmund C. JENKINS, Auteur ; Wenqiang CHEN, Auteur ; Salomon KUIZON, Auteur ; Raju K. PULLARKAT, Auteur ; Mohammed A. JUNAID, Auteur . - 2011 . - p.262-270.
Langues : Anglais (eng)
in Autism Research > 4-4 (August 2011) . - p.262-270
Mots-clés : autism glyoxalase I SNP advanced glycation endproducts (AGEs) receptor for advanced glycation end products (RAGEs) methylglyoxal Index. décimale : PER Périodiques Résumé : Autism is a pervasive, heterogeneous, neurodevelopmental disability characterized by impairments in verbal communications, reciprocal social interactions, and restricted repetitive stereotyped behaviors. Evidence suggests the involvement of multiple genetic factors in the etiology of autism, and extensive genome-wide association studies have revealed several candidate genes that bear single nucleotide polymorphisms (SNPs) in non-coding and coding regions. We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme. To identify the significance of the SNP, we have conducted functional assays for Glo1. We now present evidence that the presence of the A-allele at rs2736654 results in reduced enzyme activity. Glo1 activity is decreased in lymphoblastoid cells that are homozygous for the A allele. The Glu-isoform of Glo1 in these cells is hyperphosphorylated. Direct HPLC measurements of the glyoxalase I substrate, methylglyoxal (MG), show an increase in MG in these cells. Western blot analysis revealed elevated levels of the receptor for advanced glycation end products (RAGEs). We also show that MG is toxic to the developing neuronal cells. We suggest that accumulation of MG results in the formation of AGEs, which induce expression of the RAGE that during crucial neuronal development may be a factor in the pathology of autism. En ligne : http://dx.doi.org/10.1002/aur.197 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=141